Infections with PVL-producing Staphylococcus aureus are essentially responsible for community infections. Staphylococcus aureus expresses a large variety of virulence factors, among which is Panton-Valentine Leukocidin (PVL), a cytotoxin which promotes tissue damage1. PVL is a toxin commonly present in community acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) strains which are spreading worldwide2.
PVL, and also other leukocidins, is a protein belonging to the family of synergohymenotropic toxins. All the toxins of this family are constituted of two polypeptide components, with synergic action, denoted S and F. PVL is encoded by two cotranscribed contiguous genes, lukF-PV and lukS-PV. PVL is an exotoxin since it is excreted into the extracellular medium whether or not there has been lysis of the bacterium, unlike endotoxins or lipopolysaccharides, which, themselves, are released only when the Gram-bacterium which secretes them has been destroyed.
PVL-producing Staphylococcus aureus, which are Gram+ bacteria, are associated with specific human infections such as cutaneous infections or subcutaneous infections, of the boil, abscess, cellulitis and myositis type, osteoarticular infections, and also severe necrotizing pneumonias which affect mainly children and young adults with a mortality rate of approximately 70%.
The pathogenesis is not completely known, but several lines of evidence suggest that PVL plays an important role in the physiopathology of infections with PVL-producing Staphylococcus aureus:                 i) the strong epidemiological link with isolates of S. aureus which synthesize PVL and the clinical presentation of the infection,        ii) the high frequency of leukopenia, a known effect of PVL,        iii) the necrotic lesions of the respiratory tract, resembling the necrosis induced by intradermal injection of PVL in rabbits,        iv) the presence of PVL in the lungs targeting the polymorphonuclear cells,        v) only PVL-producing strains or purified PVL induce necrotizing pneumonia in experimental models7.        
PVL-producing S. aureus are currently detected using tests for detecting nucleic acids, and in particular by detecting the lukF-PV and lukS-PV genes by PCR3.
Such tests have the drawbacks that they are indirect since they do not make it possible to confirm that the gene is functional and/or expressed, they are expensive owing to the need for specific equipment, they are not very fast and they are difficult to carry out. In addition, in the context of the use of a PCR, contamination problems may occur.
The detection of PVL has also been carried out, from time to time, by immunodiffusion using polyclonal antibodies4, but this technique was quickly abandoned in favor of the detection of genes since it is not very easy to carry out and difficult to standardize, such that it does not constitute a good tool for routine use.
Owing to the seriousness of certain infections due to PVL-producing Staphylococcus aureus, it is becoming urgent to have available a rapid test that is simple to carry out and that would overcome the drawbacks of the tests currently used to detect PVL-producing S. aureus. 
Patent application EP 597 110 A describes the fact that the detection of MRSA can be carried out by means of routine immunological tests using anti-PVL monoclonal antibodies. However, although these tests make it possible to overcome the above drawbacks, the specificity of detection is not sufficient.